Best ITQB PhD Thesis 2012
Oeiras, 02.07.2013
Magda Atilano and Cláudia Queiroga, former ITQB PhD students, were awarded ex aequo with the Best PhD Thesis Prize 2012. The award ceremony will take place on the 5th of July, during the celebration of the ITQB Day.
For her PhD, Magda Atilano worked at the Bacterial Cell Surfaces and Pathogenesis Lab under the supervision of Sérgio Filipe. Her thesis, entitled “Bacterial peptidoglycan biosynthesis and recognition by the innate immune system”, focused on specific bacterial cell wall components and their role in the infection process. The PhD thesis public discussion took place in June 2012. Magda is now a pos-doctoral EMBO Fellow at Oxford University.
Cláudia Queiroga developed her research at the Animal Cell Technology Unit under the supervision of Helena Vieira and Paula Alves. Her work aimed to evaluate the protective role of carbon monoxide in ischemic brain stroke. The thesis, entitled "Disclosing Carbon Monoxide Protection in Cerebral Ischemia: Insights into the cellular mechanisms" was publicly presented in December 2012. After obtaining her PhD, Cláudia Queiroga moved to Centro de Doenças Crónicas (CEDOC) from the medical faculty of Universidade NOVA for her post-doc.
The award, established in 2009, aims to recognize the best PhD thesis presented at ITQB each year. The prize money of 2,000 euros is funded by Fundação Jacqueline Dias de Sousa. The selection panel includes Carlos Bandeira Duarte from Universidade de Coimbra, Mário Nuno Berberan e Santos from Universidade Técnica de Lisboa and is chaired by Cândido Pinto Ricardo from ITQB.
Summary of Magada Atilano’s PhD Thesis
Peptidoglycan (PG) is an enormous macromolecule that is specific to prokaryotes. PG enables bacteria to withstand physical stress from external forces or internal pressures. In Gram-positive bacteria, PG serves as the scaffold on which the external surface of the bacterium is assembled. PG is often regarded as a static structure when in fact it is a dynamic and highly regulated biopolymer that is continuously remodeled to allow bacterial cell growth and division. The thick PG layer of Gram-positive bacteria consists of glycan chains crosslinked by short peptides and is further modified by the presence of anionic polymers, such as teichoic acids, by the addition or removal of either N- or O- linked acetyl groups and by modulation of the degree of crosslinking between glycan chains. The pathogenic bacteria Staphyloccocus aureus has a highly modified PG. Modifications of PG confer resistance to cell wall hydrolases and could also represent a mechanism by which bacteria can counter the host immune system. During my PhD I showed that wall teichoic acids in Staphylococcus aureus, are important cell wall components involved in production of highly cross-linked peptidoglycan and in limiting the access of the PGRP-SA innate immune receptor to peptidoglycan. In addition, I revealed that wall teichoic acids are required for bacteria to establish an infection and ultimately kill the host.
Summary of Cláudia Queiroga’s PhD Thesis
Blood interruption (hypoxia-ischemia) in the brain can cause severe damage, in particular in the neonatal population, representing 23% of neonatal death worldwide. Although progresses have been made, the therapies are still limited. Carbon monoxide (CO) is known as toxic, however this is a molecule daily produced in the human body (14 mL/day) and several works have proven that in low doses it can exert protective effects. In the brain, CO effects are not totally understood. The aim of this PhD was to evaluate the role of CO in the pathological model of cerebral ischemia. Moreover, we studied how CO can protect the brain cells, disclosing important steps and players in the protective pathway. Using different models to mimick the brain and taken altogether the main results obtained, we can conclude that CO pre-treatment activates players within the cell leading to an increase on cell survival, by reinforcing cellular respiration (oxidative phosphorylation), cellular communication and impairment of, at least, one cell death pathways. In conclusion, low doses of CO are beneficial in the protection against hypoxic-ischemic damage in the brain.
